Evidence map›Paper›PMID 27551154›Full record

ArticleThe Journal of experimental medicine2016

Balance between transmitted HLA preadapted and nonassociated polymorphisms is a major determinant of HIV-1 disease progression.

Daniela C Mónaco, Dario A Dilernia, Andrew Fiore-Gartland, Tianwei Yu, Jessica L Prince, Kristine K Dennis, Kai Qin, Malinda Schaefer, Daniel T Claiborne, William Kilembe and 8 more

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of experimental medicine, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.

0numbers the graph read from it
0cells of the map it votes in
25citing papers in PubMed
3.1field-weighted citation impact, top 8% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

25 citing papers in PubMed, 42 citations in OpenAlex.

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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

18 authors at 4 institutions in 1 country.

Daniela C MónacoEmory Vaccine Center, Emory University, Atlanta, GA 30322.ORCID 0000-0002-3807-3534
Dario A DilerniaEmory Vaccine Center, Emory University, Atlanta, GA 30322.ORCID 0000-0001-8222-8655
Andrew Fiore-GartlandVaccine and Infectious Disease Division, Fred Hutchinson Cancer Research Center, Seattle, WA 98109.
Tianwei YuDepartment of Biostatistics and Bioinformatics, Emory University, Atlanta, GA 30322.ORCID 0000-0003-2502-1628
Jessica L PrinceEmory Vaccine Center, Emory University, Atlanta, GA 30322.
Kristine K DennisEmory Vaccine Center, Emory University, Atlanta, GA 30322.ORCID 0000-0003-2753-7329
Kai QinDepartment of Medicine, University of Alabama at Birmingham, Birmingham, AL 35233.ORCID 0000-0003-1721-6054
Malinda SchaeferEmory Vaccine Center, Emory University, Atlanta, GA 30322.ORCID 0000-0002-3348-3462
Daniel T ClaiborneEmory Vaccine Center, Emory University, Atlanta, GA 30322.ORCID 0000-0002-2091-1456
William KilembeZambia-Emory HIV Research Project, Lusaka, Zambia.
Jianming TangDepartment of Medicine, University of Alabama at Birmingham, Birmingham, AL 35233.ORCID 0000-0003-0137-7486
Matt A PriceInternational AIDS Vaccine Initiative (IAVI), San Francisco, CA 94105 Department of Epidemiology and Biostatistics, University of California, San Francisco, San Francisco, CA 94105.
Paul FarmerEmory Vaccine Center, Emory University, Atlanta, GA 30322.ORCID 0000-0002-4441-2264
Jill GilmourIAVI, London SW10 9NH, England, UK.
Anju BansalDepartment of Medicine, University of Alabama at Birmingham, Birmingham, AL 35233.ORCID 0000-0003-1880-4093
Susan AllenDepartment of Pathology and Laboratory Medicine, Emory University, Atlanta, GA 30322.
Paul GoepfertDepartment of Medicine, University of Alabama at Birmingham, Birmingham, AL 35233.
Eric HunterEmory Vaccine Center, Emory University, Atlanta, GA 30322 Department of Pathology and Laboratory Medicine, Emory University, Atlanta, GA 30322 ehunte4@emory.edu.ORCID 0000-0002-4273-8631
Emory University · USUniversity of Alabama at Birmingham · USFred Hutch Cancer Center · USInternational AIDS Vaccine Initiative · US

Funding

SDMC: HIV Vaccine Trials NetworkUM1AI068635 · NIAID · FRED HUTCHINSON CANCER RESEARCH CENTER · PI Peter B. Gilbert, Yunda Huang · 2011 to 2026
$385.9M
Yerkes National Primate Research Center Role of type-I IFN in regulating COVID-19 induced inflammation and pathogenesisP51OD011132 · OD · EMORY UNIVERSITY · PI Joon Sup Lee · 2012 to 2026
$167.0M
YNPRC NHP CLINICAL MEDICINE RESIDENCY PROGRAM - SUPPLEMENTP51RR000165 · NCRR · EMORY UNIVERSITY · PI ALTMAN, JOHN DAVID · 1985 to 2011
$114.0M
Virology and Molecular Biomarkers CoreP30AI050409 · NIAID · EMORY UNIVERSITY · PI Carlos del Rio · 2002 to 2026
$74.0M
CTL and HIV Polymorphisms in Heterosexual TransmissionR01AI064060 · NIAID · EMORY UNIVERSITY · PI GOEPFERT, PAUL A., HUNTER, ERIC · 2005 to 2019
$21.7M
Virologic Correlates of Heterosexual TransmissionR37AI051231 · NIAID · EMORY UNIVERSITY · PI HUNTER, ERIC · 2008 to 2017
$9.6M
A Rational Approach for HIV Vaccine T Cell Epitope SelectionR01AI112566 · NIAID · UNIVERSITY OF ALABAMA AT BIRMINGHAM · PI GOEPFERT, PAUL A. · 2014 to 2017
$1.9M
NCRR NIH HHS P51 RR000165NIAID NIH HHS P30 AI050409NIAID NIH HHS R01 AI064060NIAID NIH HHS R01 AI112566NIAID NIH HHS R37 AI051231NIAID NIH HHS UM1 AI068635NIH HHS P51 OD011132
6 · The paper itself

Abstract

HIV-1 adapts to a new host through mutations that facilitate immune escape. Here, we evaluate the impact on viral control and disease progression of transmitted polymorphisms that were either preadapted to or nonassociated with the new host's HLA. In a cohort of 169 Zambian heterosexual transmission pairs, we found that almost one-third of possible HLA-linked target sites in the transmitted virus Gag protein are already adapted, and that this transmitted preadaptation significantly reduced early immune recognition of epitopes. Transmitted preadapted and nonassociated polymorphisms showed opposing effects on set-point VL and the balance between the two was significantly associated with higher set-point VLs in a multivariable model including other risk factors. Transmitted preadaptation was also significantly associated with faster CD4 decline (<350 cells/µl) and this association was stronger after accounting for nonassociated polymorphisms, which were linked with slower CD4 decline. Overall, the relative ratio of the two classes of polymorphisms was found to be the major determinant of CD4 decline in a multivariable model including other risk factors. This study reveals that, even before an immune response is mounted in the new host, the balance of these opposing factors can significantly influence the outcome of HIV-1 infection.

Indexed as

Disease ProgressionPolymorphism, GeneticAdaptation, PhysiologicalAllelesCD4-Positive T-LymphocytesEpitopesFemalegag Gene Products, Human Immunodeficiency VirusHistocompatibility Antigens Class IHIV InfectionsHumansImmunityMaleModels, BiologicalMultivariate AnalysisT-Lymphocytes, CytotoxicEpitopesgag Gene Products, Human Immunodeficiency VirusHistocompatibility Antigens Class I

Identifiers

PMID27551154
PMCPMC5030801
OpenAlexW2511142131

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-SA
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.